Endocrinology_Medicine

Question 1

Hyponatremia - Sx? Ix & Approach? What happens if you correct Na too fast?

Answer 1

Sx: confusion, altered GCS, headaches, seizures, encephalopathic

Ix: fluid status, U&E, paired osmolalities (urine, serum)

Fluid status:

• HYPOvolaemic (dehydrated) - WASTING (diarrhoea/vomiting, diuretics) –> IV fluids
• EUvolaemic (normal) - ENDOCRINE (SIADH, hypothyroidism, Addison’s) –> fluid restrict + Tx underlying cause
• HYPERvolaemic (fluid overload) - FAILURE (liver, renal, heart) –> fluid restrict + Tx underlying cause

Urine Na:

• <20 mmol/L –> hypovolaemia (increased Na reabsorption in kidneys –> increasing H20 retention –> reducing urine Na)
• >20 mmol/L –> SIADH (BUT if on diuretics, urine Na can’t be interpreted) –> fluid restrict

Na corrected too fast (>10) = osmotic demyelination syndrome (central pontine myelinolysis) –> pseudo-bulbar palsy, paraparesis, locked-in syndrome

Question 2

Potassium homeostasis - areas involved? Hypo/hyper? Appearance on ECG? Hyper Tx?

Answer 2

Areas involved:

1. Dietary intake
2. Absorption in GI tract
3. Adrenals & kidneys - regulate serum K concentration

HYPOkalaemia:

• Poor dietary intake, vomiting/diarrhoea
• Diuretics - loop/thiazide (block channels causing K reabsorption)
• Hyperadrenalism (Conn’s, bilateral adrenal hyperplasia, Cushing’s)
  
  • Conn’s/BAH - excess aldosterone - NOTE: Aldosterone promotes reabsorption Na, excretion K
  • Cushing’s = excess cortisol –> off-target effect on mineralocorticoid receptors –> mimics aldosterone

HYPERkalaemia:

• false = HAEMOLYSIS –> repeat sample
• Kidney failure e.g. on dialysis (kidneys = main route to remove K)
• Anti-HTN/diuretics
  
  • ACEi/ARB - reduce kidney hyperfiltration, mainly a risk if CKD
  • K⁺-sparing diuretics e.g. spironolactone/amiloride
• Addison’s disease (failure - can’t produce enough cortisol/aldosterone)
• NOTE: appearance on ECG = tented T-waves, broad QRS, prolonged PR interval

Hyperkalaemia Tx:

• Protect heart - IV 10-30ml 10% Ca Gluconate (repeat /15m, x5 MAX)
• Reduce K⁺:
  
  • 1st line - 10U Actrapid (insulin > drive K into cells) AND 100mL 20% glucose (to prevent hypo)
  • 2nd line - 5mg Salbutamol NEB (b-agonist)
• Ix cause: drug chart, U&E (kidney funct), short SynACTHen test (Addison’s)

Question 3

Calcium homeostasis?

Hyper Sx? Ix & causes? Mx?

Hypo Causes? Sx? Ix? Mx?

Answer 3

Hormone production:

• Parathyroid gland - PTH –> INCREASE Ca:
  
  • Bone resorption
  • GI absorption
  • Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
• Vit D₃ aka cholecalciferol (UV)/ergocalciferol (diet)
  
  • In Liver –> 25-OH(D) aka calcidiol
  • In Kidney + 1alpha-hydroxylase –> 1,25-OH₂(D) aka Calcitriol (activated vitD) –> INCREASE Ca
    
    • GI absorption
    • Kidney - decreased excretion

HYPERcalcemia ​

• Sx:
  
  • Stones - urinary tract calculi
  • Bones - fractures
  • (Abdo) moans - dyspepsia
  • Thrones - polyuria, constipation
  • (Psych) overtones - depression, psychosis
• Ix - check PTH:
  
  • Low - hypercalcemia of malignancy (PTH axis is functioning normally) - bone mets, PTHrP (released by lung SCC), myeloma (CRAB)
  • Normal/high - primary hyperparathyroidism (as if serum Ca high, PTH should be low) - adenoma, hyperplasia, MEN 1&2
  • Other:
    
    • Fluid status, ECG (short QT), protein electrophoresis, 24hr urinary Ca (familial hypocalciuric hypercalcemia)
    • Bloods - bone profile (Ca, PO4), U&E
    • Imaging: CXR
• Mx:
  
  • IMMEDIATE = aggressive IV 0.9% fluid resus (4-6L over 24krs), repeat Ca
  • Tx underlying cause:
    
    • Parathyroid adenoma - minimally invasive surgery (subtotal/total parathyroidectomy)
    • Malig - Zalendronate/Pamidronate (inhibit osteoclast activity), slow infusion
    • Other:
      
      • If bone mets –> bisphosphonates
      • If renal failure –> Cinacalcet (reduce PTH)
  • Recheck serum Ca @day 2 –> 4

HYPOcalcaemia

• Causes:
  
  • Hypoparathyroidism (PO4 high, PTH low)
  • Pseudohypoparathyroidism (PO4 high, PTH high) = PTH resistance
  • CKD (high PO4, PTH high, ALP high)
  • Vit D def (rickets/osteomalacia, low/normal PO4, high PTH, high ALP)
  • Hypomagnesaemia (low/normal PO4, low/normal PTH, normal ALP)
• Presentation:
  
  • Peri-oral numbness, digital paraesthesia, dermatitis
  • +ve Trousseau’s (BP cuff 20 over SBP for 3mins –> salt bae hand), Chovstek signs (tap over the masseter muscle in the inferior pre-auricular area)
  • Laryngospasm (wheeze, dysphagia, muscle cramps)
  • Confusion, seizures, prolonged QT
• Ix: serum Ca, PO4, Mg, PTH, U&E, Vit D
• Mx: PO/IV replacement of Ca

Question 4

Hyperparathyroidism sub-categories?

Answer 4

• Primary - PTH secretion from primary parathyroid tumour/ectopic secretion from another tumour (high Ca, high PTH)
• Secondary - PT hyperplasia to maintain control of hypocalcemia, normally from CKD (low Ca, high PTH, normal -ve feedback)
  
  • CKD –> bone profile, parathyroid hormone lvl every 3-6 months
• Tertiary - prolonged secondary, becomes irrepressible by serum Ca lvls. Mostly kidney transplant patients (high Ca, very high PTH)

Question 5

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?

Answer 5

Presentation: polyuria, polydipsia, dehydration

• Ketosis - malaise, vomiting
• FHx, other endo disorders
• If known DM:
  
  • Previous DM control (hyp/hyper)
  • Micro/macrovascular complications
  • Diabetic eye disease (Dx & Tx)

RFs: overweight, FHx (DM), PMHx (GDM), PCOS, HTN, dyslipidemia, CVD

Criteria for Dx (repeat test needed for Dx):

• Fasting plasma glucose of ≥7.0 (normal ≤6)
• OGTT (BM 2hours after 75g glucose-load)/ Sx + random plasma glucose of ≥11.1mmol/l (normal <7.8)
• HbA1c ≥48mmol/mol (≥6.5%) - not for young/T1DM, acutely ill, haem disease, preg, iatrogenic

T1DM Mx: exogenous insulin to avoid DKA & long-term complications

• Diet - lower fat, higher carbs = counting carbs (adjust insulin around diet rather than limiting eating)
• Diabetic specialist nurse - EDUCATE:
  
  • Self-adjust dose - DAFNE course for T1DM (D for DM)
  • Fingerprick glucose
  • Calorie intake & carb counting
  • Phone support
• Don’t stop insulin during acute illness, maintain calorie intake
• Insulin regimens:
  
  • 1st line - Basal-bolus regimen
    
    • Basal (background) - BD insulin detemir (or Levemir/Lantus/Tresiba) as basal insulin
    • Bolus (before meals) - analogue rapid-acting insulin e.g. insulin Lispro (Humalog)/Aspart (Novorapid)/Neutral (Actrapid)
  • Other:
    
    • BD biphasic (premixed insulin, hypos common) e.g. Novomix, Humulin M3, Humalog Mix
    • OD before bed long-acting (for T2DM)
    • NOTE: intermediate-acting insulin e.g. Humulin I, Insulatard

T2DM Mx:

• 1st line - Lifestyle changes - DESMOND course for T2DM (D for DM), dietician input, self-BM monitoring (individual HbA1c target <6.5)
  
  • HbA1c targets:
    
    • No hypoglycaemics - 48mmol/mol
    • Hypoglycaemics - 53mmol/mol
    • Escalate Tx - 58mmol/mol
• Medication:
  
  • 2nd - Metformin (SEs: diarrhoea, LA - avoid if eGFR <30)
  • 3rd - ADD Sulphonylurea e.g. Gliclazide (SEs: hypoglycaemia, weight gain)
  • 4th - ADD other DM med:
    
    • Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
      
      • C/I in HF, bladder cancer
    • SGLT-2 inhibitor e.g. Empagliflozin (SEs: Hypoglycaemia, weight loss, UTI)
      
      • Not recommended in impaired renal funct
    • DPP-4 inhibitor e.g. Linagliptin (APPROVED FOR USE IN CKD, weight neutral)
    • GLP-1 analogues e.g. Exenatide/Liraglutide (SE: weight loss - useful if BMI >35; vomiting)
      
      • Not recommended in impaired renal funct
  • 5th - If on triple therapy & not providing control –> commence insulin
• CVD risk Mx - anti-HTN, anti-lipid, QRISK-3 score
• Diabetic nephropathy Mx:
  
  • Monitor albumin-creatinine ratio (ACR)
  • Consider ACEi/ARB early
• Diabetic neuropathy Mx:
  
  • Annual Sx review (erectile dysfunction, autonomic neuropathy - orthostatic hypotension, gastroparesis, bladder emptying difficulties)
  • Annual foot screen + specialist foot Mx, monitor for diabetic foot/ulcers ± amputation
• Diabetic retinopathy: retinal screen annually (age ≥12yrs)
  
  • Background: need to tighten control
    
    • Venodilation, microaneurysms (dots), hard exudates (lipid deposits)
    • Tx: tighten glycaemic control, refer if near macula
  • Pre-proliferative (mild) - soft exudates (cotton wool spots e.g. infarcts)
  • Proliferative - neovascularization (+ floaters, reduced acuity)
    
    • Tx: pan-retinal photocoagulation
  • Diabetic maculopathy - hard exudates, oedema (+ blurred vision, reduced acuity)
    
    • Tx: intravitreal triamcinolone acetonide decreases macula oedema
  • NOTE: Pre-diabetic –> refer to diabetes prevention programme (DPP)

Diabetes complications:

• Microvascular:
  
  • Eye - diabetic retinopathy (± cataracts, glaucoma)
  • Kidney - diabetic nephropathy
  • Neuropathy - damage to PNS –> diabetic neuropathy (peripheral neuropathy - glove & stockings distribution) –> diabetic ulcers/gangrene
• Macrovascular:
  
  • Brain - stroke/TIA/cog impairment
  • Heart - coronary heart disease
  • Extremities - PVD, diabetic ulcers/gangrene

Question 6

Acromegaly cause? presentation? Ix? Mx? Complications?

Answer 6

Cause: macroadenoma in anterior pituitary

Presentation: coarse facial features

• Skin (acanthosis nigricans - thick & dark in creases), sweating, carpal tunnel syndrome (bilateral)
• Arthropathy, sleep apnoea, reduced sexual functioning, visual field defects (bitemporal hemianopia)
• Assoc: DM, HTN, MEN type 1 (15%)

Ix:

• Bedside: CN VI palsy, urine dip (glucose), ECG (cardiomyopathy)
• Bloods: elevated IGF-1, GH lvl during OGTT (not suppressed in acromegaly)
• Imaging: MRI brain (macroadenoma), sleep studies, colonoscopy (screening), visual field testing (driving)

Mx:

• Transsphenoidal hypophysectomy (curative)
• Medical: somatostatin analogue (octreotide)
• External pituitary radiotherapy (long-term 5-10yrs)

Complications:

• General: HTN, DM, carpal tunnel syndrome, sleep apnoea, colorectal cancer, LVH/cardiomyopathy/IHD
• Anterior pituitary hypofunction: hypogonadism
• Local compressive: bitemporal hemianopia

Question 8

Hyperosmolar Hyperglycaemic State

• What does insulin do? Pathophysiology of HHS?
• HHS criteria? HHS Mx? HHS Mx Targets?

Answer 8

Insulin:

• High level of insulin –> reduces serum BM (pushes into surrounding tissues & hepatic glucose store)
• Low level of insulin –> switches off ketone production

Pathophysiology:

• HHS = complication of T2DM
• In HHS have enough insulin to switch of ketone production but not enough to reduce BM lvls
• High glucose - osmotically active –> polyuria –> dehydration

HHS criteria:

• Hypovolaemia
• Glucose >30mmol/L
• NO ketonaemia
• Serum osmolality >320mOsmol/kg

Mx: REHYDRATE = IV 0.9% NaCl (3-6L by 12hrs, deficit 110-220mL/kg)

• Targets:
  
  • Reduce Na by less than 10mmol/L/day (otherwise risk osmotic demyelination syndrome)
  • Reduce BM by over 5mmol/L/hr
  • NOTE: if targets not met by 0.9% saline –> 0.45% instead
• If fluid alone are not enough –> 0.05 units/kg/hr fixed-rate insulin infusion

Question 9

SIADH - pathophysiology? criteria? causes?

Answer 9

Criteria:

• True hyponatraemia
• High urine osmolality
• Clinically euvolemic
• Dx of exclusion (9am cortisol + TFTs must be normal)

Causes:

• Malig (small cell lung cancer, breast cancer)
• CNS disorders (encephalitis, abscess)
• Chest disease (pneumonia, TB)
• Drugs (opiates, SSRIs, carbamazepine)

Question 10

Diabetes insipidus - Sx? Types? Ix? Tx?

Answer 10

Sx: hypernatremia (lethargy, thirst, irritable, confusion, coma, fits), polyuria, urine plasma osmolality <2 (very dilute)

Types:

• Central (lack of ADH prod in hypothalamus) – pituitary surgery, irradiation, trauma, infarction
• Nephrogenic (resistance to ADH effects) – hypercalcaemia, hypokalaemia, meds (lithium)

Ix: rule out DDx (BM, review drugs, K/Ca lvls)

• U&E, Ca, BM, serum & urine osmolarities
• Dx: 2-step fluid deprivation test = give desmopressin (DDAVP):
  
  • Normal/primary polydipsia –> urine concentrates on fluid deprivation (>600)
  • Cranial DI - giving desmopressin allows ADH prod –> urine conc
  • Nephrogenic DI: urine never concentrates
  • NOTE: DI excluded if urine to plasma (U: P) osmolarity ratio >2:1
• Cranial MRI - if suspect cranial DI

NOTE: Fluid deprivation test process:

• Baseline urine osmolality
• Fluid deprivation for 8hrs, take urine osmolality
• Give desmopressin, wait 8hrs, take urine osmolality

Tx:

• Nephrogenic DI –> fluids (+ monitor UO) + thiazide diuretics (hydrochlorothiazide - weird/does not make sense)
• Central DI –> fluids + desmopressin

Question 11

Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?

Answer 11

Hypothyroidism:

• Causes:
  
  • Primary:
    
    • Hashimoto’s thyroiditis - most common hypothyroidism
      
      • Goitre, AI disease (vitiligo, pernicious anaemia, T1DM, Addison’s)
      • Elderly females
      • May be initial ‘Hashitoxicosis’
      • +++ Autoantibody titres
        
        • Antithyroid peroxidase (TPO) & antithyroglobulin (TG)
    • Atrophic AI thyroiditis
      
      • No goitre, anti-TPO/TSH
    • Iodine def, meds (carbimazole, lithium), thyroid surgery
  • Secondary: pituitary gland fails to produce TSH
    
    • Tumour, vascular (Sheehan syndrome), radiation, inf
• Ix:
  
  • Bedside: ECG (pericardial effusion, ischaemia)
  • Bloods: FBC, U&E, TFTs, Lipids, Prolactin, Anti-TPO/TG
  • Imaging: CXR (effusions, HF)
• Mx: thyroid replacement therapy (levothyroxine)
  
  • Monitor with serum TSH, careful with dose in elderly (prone to IHD)
  • Myxoedema coma - A-E & active warming, T3 slow IV, hydrocortisone IV
• Associated complications:
  
  • Cardiac - HF
  • Serous effusions (pleural, peritoneal, pericardial, joint)
  • Neuro - carpal tunnel, proximal myopathy, cerebellar dysfunction, myxedema coma
  • Systemic - dyslipidemia, anaemia

Hyperthyroidism:

• Presentation:
  
  • Weight loss, increased appetite
  • Heat intolerance, tremor, sweating, palpitations
  • Mood (anxious, irritable)
  • Bowel habit (diarrhoea), menses (oligomenorrhoea)
  • Goitre
  • Eye Sx (watering, gritty, red)
  • Other AI disease (vitiligo)
  • Signs:
    
    • Lid lag (eyes)
    • Palmar erythema
    • Brisk reflexes
    • Sinus tachy/AF
• Ix: TSH low, T3/4 high, TPO (may be raised), anti-TSHr ab (in Graves), technetium 99m uptake scan (diffuse/reduced)
• Causes:
  
  • High-uptake:
    
    • Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
      
      • Eye signs: proptosis –> exophthalmos, diplopia, visual loss
      • Peripheral signs: pretibial myxoedema, thyroid acropatchy, onycholysis, bruit over thyroid
    • Toxic multinodular goitre aka Plummer’s disease: hot nodules, painless
    • Toxic adenoma: 5%, single ‘hot nodule’ on isotope scan (1 area of uptake)
  • Low-uptake:
    
    • Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
      
      • Tx: NSAIDs
    • Postpartum thyroiditis (like De Quervain’s but postpartum)
• Mx:
  
  • Conservative: lifestyle changes, corneal lubricants
  • Medical:
    
    • Sx relief – B-blockers
    • Antithyroid meds - Carbimazole (or propylthiouracil)
      
      • SEs: rashes, agranulocytosis - monitor​
    • Radioiodine:
      
      • acts slowly, effective, best Tx for toxic multinodular goitre
      • Risk of permanent hypothyroidism (10%)
      • CI in preg/lactating women
  • Surgical: subtotal thyroidectomy (in large goitre/relapse)
  • Monitoring with TFTs annually
  • Thyroid storm: acute state of shock, pyrexia, confusion, vomiting
    
    • HDU/ITU support
    • Propylthiouracil 600mg –> 200mg QDS
    • Stable iodine (Lugol’s iodine) ≥1hr later
    • Propranolol, dexamethasone & IV fluids

Question 12

Adrenal disease breakdown? Causes? Presentations? Ix? Mx?

Answer 12

Cushing’s #HighCortisol

• Causes:
  
  • ACTH-dependent:
    
    • Pituitary tumour (85%) = “Cushing’s disease”
    • Ectopic ACTH-prod tumour (5%) - SCLC/carcinoid tumour
  • ACTH-independent:
    
    • Adrenal tumour (10%)
    • Iatrogenic steroid use
• Presentation:
  
  • Thin skin, easy bruising, proximal myopathy, obesity (moon face, buffalo hump), other (hirsutism, acne)
  • Exam: vertical abdo striae
  • HTN, DM, osteoporosis (back/bone pain)
• Ix:
  
  • Exclude pseudo-Cushing’s - depression, alcohol excess, chr inf (no muscle weakness)
  • Confirm Dx: low-dose dex suppression test - fail to suppress cortisol in all
    
    • Overnight dexamethasone suppression test (1g @11pm) OR
    • 48hr low-dose 0.5mg/6h PO dexamethasone supression test OR
    • 24-hr urinary free cortisol (test x3 as low sensitivity)
  • Plasma ACTH measured:
    
    • High - CRH test identifies if pituitary or ectopic
      
      • Could also do bilateral inferior petrosal sinus sampling –> if no mass –> CT contrast CAP for ectopic
    • Low - adrenal tumour –> CT/MRI adrenal glands –> if nothing –> adrenal vein sampling
• Mx: treat underlying disease e.g. withhold steroids or surgical removal of the lesion
  
  • Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
    
    • 2nd - pituitary radiotherapy (also used if still high cortisol post-surgery) –> progressive anterior pituitary failure
    • Metyrapone & ketoconazole - sometimes before/after surgery
    • 3rd - laparoscopic bilateral adrenalectomy in refractory (but require lifelong glucocorticoid/mineralocorticoid replacement + risk of Nelson’s syndrome (increased skin pigment from high ACTH

Hypoadrenalism

• Causes:
  
  • AI: Addison’s disease (>70%)
  • Malig: mets (lung, breast. kidney)
  • Inf: TB (>10%), HIV (CMV adrenalitis), Fungal
  • Infiltration: granulomatous disease, hemochromatosis, amyloidosis
  • Iatrogenic: ketoconazole, rifampicin, phenytoin, bilateral adrenalectomy
  • Congenital: congenital adrenal hyperplasia (late-onset)
• Presentation:
  
  • Anorexia/weight loss, fatigue/weakness, postural dizziness, reduced libido, sweating
  • N&V, diarrhoea, salt craving
  • Signs: hyperpigmentation in skin creases/lip/mouth, vitiligo, sparse axillary/pubic hair
• Ix:
  
  • Bedside - postural hypotension, IGRA (TB inf)
  • Bloods - FBC, U&E (↑ K⁺, ↓ Na⁺), low glucose, serum Ca, AI/auto-ab screen, plasma renin & aldosterone, short snACTHen 250mcg IM test (not Addison’s if 30min cortisol rises >550nmol/L
  • Imaging: CXR (past TB), adrenal CT (for TB/mets)
• Mx:
  
  • Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
    
    • Ppt factors: inf, trauma, surgery, missed steroid doses
    • Ix: Cortisol, ACTH, U&E
    • Mx: IV hydrocortisone + IV fluids ± fludrocortisone (if primary adrenal lesion)
      
      • Monitor BM ± IV dextrose
      • Bloods, urine, sputum culture ± abx
  • Chronic: hydrocortisone + fludrocortisone (Na homeostasis), education (compliance, increase steroid dose if ppt factors, follow-up

Hyperaldosteronism (incl. Conn’s)

• Primary (HTN, ↑ Na+ ↓ K+):
  
  • ​Conn’s - aldosterone-secreting adrenal adenoma
  • Bilateral adrenal hyperplasia
• Secondary - decreased renal perfusion (high renin –> Na reabsorption –> HTN) - RAS, HF, liver failure
• Ix: aldosterone-renin ratio (ARR), CT/MRI adrenals, adrenal vein sampling
  
  • Conn’s is very high (high aldosterone, low renin) VS BAH has both high (high aldosterone, high renin)
• Mx: spironolactone, unilateral adrenalectomy (for Conn’s)

PHaeochromocytoma #HighCatecholamines

• Cause: adrenal medulla tumour –>↑ catecholamines (adrenaline/NA)
• Presentation: episodic headache, sweating, tachycardia, hypertension, arrhythmias, death if untreated
• 10% exta-adrenal, 10% bilateral, 10% malignant
• Ix: ECG (LVF, increased ST seg, VT), 24hr urinary metanephrines, abdo CT/MRI
• Mx: specialist endo centre - alpha blockade = PHenoxybenzamine then beta-blockade –> then surgery when BP controlled (after 4-6wks)

Question 13

Mx of obesity?

Answer 13

• Conservative measures
• Medical (none proven to provide sustainable weight loss)
  
  • Orlistat (gut lipase inhibitor, SEs: profound flatus, diarrhoea)
• Surgical – bariatric surgery (BMI >40 OR >35 w/ comorbidity assoc w/ obesity)
  
  • Needs extensive screening + commitment to long-term follow-up

Question 14

Hyperprolactinaemia - causes? presentation? Ix? Mx

Answer 14

Causes:

• Prolactinoma (macroprolactinoma >6000)
• Adenoma (non-funct pituitary adenoma 1000-5000, from compression & DA lvls)
• DA antagonist (metoclopramide, anti-psychotics, methyldopa)
• Hypothyroidism (increased TRH stimulates prolactin prod)
• Physiological (pregnancy, breastfeeding)

Presentation: irreg periods, decreased libido, galactorrhoea

• Bilateral hemianopia

Ix:

• Bedside - pregnancy test, visual fields assessment
• Bloods - serum prolactin, TFTs, U&E
• Imaging - pituitary MRI

Mx:

• Asymptomatic pre-menopausal/post-menopausal with microadenoma - observation
• Symptomatic pre-menopausal/macroadenoma post-menopausal/male:
  
  • Dopamine agonist (Cabergoline/Bromocriptine), 2nd line - COCP (not if want pregnancy)
  • Trans-sphenoidal surgery (if visual Sx/pressure effects refractory to medical Tx)
  • Follow-up: monitor prolactin, check visual fields

Question 15

DDx for tiredness & lethargy? Ix?

Answer 15

DDx:

• Anaemia - PUD, altered bowel habit? occult blood loss?
• Thyroid disease - thyroiditis?
• DM - polyuria, polydipsia, weight loss
• Adrenal insufficiency
• Primary hyperparathyroidism - constipation, urinary stones, abdo pain, depression
• Hypopituitarism
• Anxiety & depression - sleep disturbances, poor appetite, recent stress

Ix:

• FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics
• CXR

Question 16

DDx for weight loss?

Answer 16

DDx:

• Thyrotoxicosis - heat intolerance, palpitations, SoB, mood (irritable/anxious), bowel habit, menses, goitre, exophthalmos, recent pregnancy
• GI-related conditions (IBD, upper GI pathology, coeliac disease, chr pancreatitis) - dysphagia, vomiting, regurgitation, abdo pain, altered bowel habit
• Eating disorders (Anorexia nervosa) - reduced eating, compulsive exercise
• Systemic conditions (malignancy) - FLAWS

Ix:

• FBC, U&E, CRP, LFTs, fasting BM, bone profile, TFTs, anti-TTG, IgA levels, haematinics
• CXR

Question 17

What are the causes of goitre?

Answer 17

Diffuse: Graves’ disease, Hashimoto’s thyroiditis, De Quervain’s thyroiditis

Nodular: Multinodular goitre, adenoma, carcinoma

Question 18

Diabetic Ketoacidosis (DKA)

• Normal glucose transport & during starvation?
• The problem in insulin deficiency (diabetes)? How does this relate to Sx of DKA?
• Ix? Dx criteria? Mx? Monitoring Tx & hourly targets?

Answer 18

Normal glucose transport: diet –> blood –insulin–> hepatic glucose store –GH, Cortisol, Adrenaline, Glucagon–> blood

• During starvating - GH, Cortisol, Adrenaline, Glucagon make sure there is enough glucose in the blood BUT liver also produces ketones
• Ketones can cross BBB providing an alternative source of fuel for the brain when low glucose
• Pancreatic beta cells –> insulin prod –> reduces glucose (high glucose has–> feedback on pancreatic beta cells –> produce more insulin)
• High insulin (associated with high glucose) –> -ve feedback on ketone prod

In insulin deficiency - high glucose but unable to produce insulin + no -ve feedback on ketone prod –> high glucose, high ketones

• High glucose - osmotically active (moves along concentration gradient into urine –> pulling more water with it) –> POLYURIA –> DEHYDRATION
• High ketones - acidic (metabolic acidosis) –> enzyme dysfunction –> COMA & DEATH

DKA Ix:

• Bedside - urine dip, ECG, continuous cardiac monitoring
• Bloods - VBG, FBC, U&E, BC, BM
• Imaging - possibly CXR

DKA Dx:

• BM: ≥11mmol/L
• Ketones: ≥3mmol/L (serum) OR ≥2+ (urine)
• Acidaemia: pH <7.3 OR Bicarb <15mmol (ketoacidosis)

DKA Mx: A-E assessment

• IV FLUIDS (rehydrate)
  
  • ​Bolus –> 1L over 1hr –> 2hr –> 3hr –> 4hr
  • Add 40mmol KCL to fluids after bolus
• 0.1 U/kg/hr fixed-rate INSULIN infusion (reduce ketones)
  
  • If BM <14 –> start 125ml/hr 10% dextrose
  • Insulin infusion continues until ketones normalise (not BM) ​
• NOTE: follow local trust guidelines for DKA Tx as varies slightly between trusts

Monitor - BM, ketones, VBG (K conc)

• Hourly targets:
  
  • Fall in BM ≥3
  • Fall in ketones ≥0.5
  • Rise in HCO3 ≥3
• Continue until: blood ketones <0.6, pH >7.3, HCO3 >18